Dujić, Željko

Respiratory muscle fatigue could occur following involuntary breathing movements during maximal breath-holds. We measured respiratory muscle strength pre and post three preparatory and maximal breath-holds. We found significant reductions in diaphragm strength and total inspiratory and expiratory strength in some, but not all, divers. Divers that had respiratory muscle fatigue had a lower pseudo O 2 delivery (HR × [Formula: see text]) during the struggle phase. This suggests that reduced oxygen delivery may contribute to respiratory muscle fatigue during a breath-hold.

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnea and congestive heart disease patients. Ventilatory response to hypercapnia and/or hypoxia is blunted in apnea divers, whereas cerebrovascular reactivity to hypercapnia is presently unknown. We hypothesized that cerebrovascular reactivity to hypercapnia is increased in elite apnea divers, compared to control subjects, as a part of the O 2 conserving mechanism to maintain adequate brain O 2 supply. In the present study we determined cerebrovascular reactivity by measuring change in middle cerebral artery velocity per mmHg change in P ET CO 2 in response to two hyperoxic hypercapnia rebreathing maneuvers in seven elite apnea divers and seven control subjects. Ventilatory response to hypercapnia was blunted in divers compared to controls. Hypercapnia‐induced ventilation increase was significantly lower in divers due to lower respiratory frequency. Cerebrovascular reactivity was unchanged in both groups (3.7±1.4 vs 3.4±1.3 %/mmHg P ET CO 2 in divers and controls) and the same was found for cerebral vascular resistance and a time for middle cerebral artery velocity recovery to baseline value. Results indicate that the regulation of the cerebral circulation in response to hypercapnia shows no difference between divers and controls serving as protective mechanism against chronic intermittent cerebral hypoxia/hypercapnia. This study was supported by Croatian Ministry of Science, Education and Sports.

Involuntary apnea during sleep elicits sustained arterial hypertension through sympathetic activation; however, little is known about voluntary apnea, particularly in elite athletes. Their physiological adjustments are largely unknown. We measured blood pressure, heart rate, hemoglobin oxygen saturation, muscle sympathetic nerve activity, and vascular resistance before and during maximal end-inspiratory breath holds in 20 elite divers and in 15 matched control subjects. At baseline, arterial pressure and heart rate were similar in both groups. Maximal apnea time was longer in divers (1.7±0.4 versus 3.9±1.1 minutes; P <0.0001), and it was accompanied by marked oxygen desaturation (97.6±0.7% versus 77.6±13.9%; P <0.0001). At the end of apnea, divers showed a >5-fold greater muscle sympathetic nerve activity increase ( P <0.01) with a massively increased pressor response compared with control subjects (9±5 versus 32±15 mm Hg; P <0.001). Vascular resistance increased in both groups, but more so in divers (79±46% versus 140±82%; P <0.01). Heart rate did not change in either group. The rise in muscle sympathetic nerve activity correlated with oxygen desaturation ( r 2 =0.26; P <0.01) and with the increase in mean arterial pressure ( r 2 =0.40; P <0.0001). In elite divers, breath holds for several minutes result in an excessive chemoreflex activation of sympathetic vasoconstrictor activity. Extensive sympathetically mediated peripheral vasoconstriction may help to maintain adequate oxygen supply to vital organs under asphyxic conditions that untrained subjects are not able to tolerate voluntarily. Our results are relevant to conditions featuring periodic apnea.